A study identifies a key mechanism in the way that the liver processes the acute and fat, which has direct implications in diseases such as diabetes, obesity and metabolic liver disease. Understanding the role of this mechanism, which exercises as a key “sensor” during the transition from aid to food, and doing it from a physiologic point of view, could open new therapeutic pathways to improve the control of glucose and body capacity to adapt to changes between aid and food. This is especially relevant in diseases such as those described above, since the horse loses precisely this capacity. The study promoted by the IRB CatSud, formerly IISPV) and led by researchers from the area of Diabetes and Associated Metabolic Diseases (CIBERDEM), has been published in the scientific journal Science Advances with the title SUCNR1 coordinates metabolic flux, mitochondrial function, and nutrient-dependent adaptation in hepatocytes. Researchers from various areas of the Consorcio Centro de Investigación Biomédica en Red) (CIBER) of the Instituto de Salud Carlos III (ISCIII) and the Universitat Rovira i Virgili (URV), have participated in the study.
The Diabetes and Associated Metabolic Diseases (DIAMET) research group at IRB CatSud is responsible for the study that provides relevant knowledge to advance in the prevention and treatment of high-impact metabolic disorders in public health in the long term. The research team has focused on succinate, which apart from serving to obtain energy, also acts as a signal in other cells through a receptor called SUCNR1. This receptor is especially abundant in a specific area of the hygro and increases during the development of this organ, which suggests an important role in liver function.
In addition, the research staff has discovered that both the levels of succino and the expression of the SUCNR1 receptor in the liver varied depending on whether the organism is in aid or fed. To better understand their role, the researchers involved studied mice that lack this receptor in the main cells of the hygda (the hepatocytes). In the absence of this receptor, the liver “is active in excess” and ends up producing more glucose than necessary in conditions of aid. This is accompanied by a lower capacity of the organism to adapt correctly to the changes that derive from the nutritional state, that is, in aid or after eating. At the cellular level, the lack of this receptor alters the way in which the water cells use glucose to produce energy, which causes the dependence of other nutrients and alters their functionality. Consequently, in response to the intake, an incomplete recovery of the energy reserves of the cells is observed.
Together, these results identify the SUCNR1 regulator as essential in the metabolic adaptation of the water, connecting energy signals with the capacity of cells to adjust to nutritional changes.
The study involved the participation of other research centres and universities, such as the Centro Singular de Investigación en Medicina Molecular y Enfermedades Crónicas (CIMUS), Universidad de Santiago de Compostela, the Institut de Recerca Biomèdica Barcelona (IRB Barcelona), the Universitat de Barcelona (UB), the Centro Nacional de Investigaciones Oncológicas (CNIO), the Institut de Recerca Sant Pau, the Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), the University of Bern and the Bern University Hospital. Also have participated reseachers of the CIBER de Fisiopatología de la Obesidad y Nutrición (CIBEROBN) and CIBER de Enfermedades Hepáticas y Digestivas (CIBEREHD).
Bibliographic reference
Marsal-Beltran, A., Salmerón-Pelado, L., Ribas-Latre, A., Repollés-de-Dalmau, M., Rodríguez-Peña, M. M., Núñez-Roa, C., Badia, J., Madeira, A., Novoa, E., Beltrà, M., Plata-Gómez, A. B., Capellades, J., Escolà-Gil, J. C., Zorzano, A., Yanes, Ó., Efeyan, A., Nogueiras, R., Gracia-Sancho, J., Vendrell, J., Ceperuelo-Mallafré, V., … Fernández-Veledo, S. (2026). SUCNR1 coordinates metabolic flux, mitochondrial function, and nutrient-dependent adaptation in hepatocytes. Science advances, 12(24), eaec8873. https://doi.org/10.1126/sciadv.aec8873
A research study based on the analysis of genetic data from hundreds of thousands of people has identified previously hidden genetic links between Autism Spectrum Disorder (ASD) and several cardiometabolic diseases, such as obesity, type 2 diabetes and high cholesterol. These findings, published in the prestigious scientific journal Molecular Psychiatry, help explain why people with autism have a higher risk of developing physical health problems throughout their lives.
D’esquerra a dreta, Elisabet Vilella, Maria Guardiola-Ripoll i Gerard Muntané
The study was carried out by researchers from the Hospital Universitari Institut Pere Mata (HUIPM) and the Institut de Recerca Biomèdica Catalunya Sud (IRB CatSud, formerly IISPV), in collaboration with the University of Oslo, and with the participation of the Rovira i Virgili University (URV).
The results show that some of the same genetic factors that influence autism are also involved in metabolic disorders, such as weight gain and diabetes, and in the same direction. This suggests that there are shared biological mechanisms linking mental health and physical health. However, when cardiovascular health factors such as blood pressure are analysed, the relationship is more complex. In these cases, the same genetic factors may have opposite effects, suggesting that different and still poorly understood mechanisms are involved.
Researchers have also identified more than one hundred regions of the genome involved in these connections, opening up new ways to better understand how the brain and the body interact.
“More and more evidence shows that mental health and physical health cannot be understood separately, and this type of study brings us closer to more personalised medicine that takes into account all the factors influencing people’s health,” says Gerard Muntané, first author of the article.
Experts highlight that these results could help, in the future, to detect physical health risks in people with autism earlier and to design more effective prevention strategies.
Article reference
Muntané, G., Shadrin, A., Guardiola-Ripoll, M., O’Connell, K. S., Frei, O., Naerland, T., Vilella, E., & Andreassen, O. A. (2026). Genetic overlap and shared risk loci between autism spectrum disorder and cardiometabolic traits. Molecular Psychiatry. https://doi.org/10.1038/s41380-026-03563-x